Termination of phase 2 of the action potential plateau occurs when time-dependent, voltage-dependent, and in-tracellular Ca++-dependent inactivation of ICa++ results in the unopposed repolarizing effects of the outward K+ currents. The combination of these effects results in rapid repolarization with a return to the hyperpolarized resting membrane potential. Pharmacological interventions that inhibit IK prolong the membrane action potential by de laying repolarization. Mutations in the genes encoding the various subtypes of IK inhibit proper channel function and result in the LQTS.
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